[Echogram of normal mitral valve and the mitral valve in mitral valve stenosis].
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OBJECTIVE: To determine predictors of systolic anterior motion and left ventricular outflow tract obstruction (SAM/LVOTO) after mitral valve repair (MVRep) in patients with myxomatous mitral valve disease. BACKGROUND: Mechanisms for the development of SAM/LVOTO after MVRep have been described; however, predictors of this complication have not been explored. We hypothesize that pre-MVRep transesophageal echocardiography (TEE) can predict postrepair SAM/ LVOTO. METHODS: Using TEE, the lengths of the coapted anterior (AL) and posterior (PL) leaflets and the distance from the coaptation point to the septum (C-Sept) were measured before and after MVRep in 33 patients, including 11 who developed SAM/LVOTO (Group 1) and 22 who did not (Group 2). RESULTS: Group 1 patients had smaller AL/PL ratios (0.99 vs. 1.95, p < 0.0001) and C-Sept distances (2.53 vs. 3.01 cm, p = 0.012) prior to MVRep than those in Group 2. Resolution of SAM/LVOTO was associated with increases in AL/PL ratio and C-Sept distance. This reflects a more anterior position of the coaptation point in those who developed SAM/ LVOTO. CONCLUSIONS: These data suggest that TEE analysis of the mitral apparatus can identify patients likely to develop SAM/LVOTO after MVRep for myxomatous valve disease. The findings are consistent with the concept that SAM of mitral leaflets is due to anterior malposition of slack mitral leaflet portions into the LVOT. The position of the coaptation point of the mitral leaflets is dynamic and a potential target and end point for surgical designs to prevent SAM/LVOTO post MVRep.
A four month old infant was investigated for heart failure was found to have mitral incompetence and severe subvalvar aortic stenosis. The left ventricular outflow tract obstruction was found to be due to an anatomically anomalous mitral valve. The obstruction could only be relieved by removal of the mitral valve and its replacement with a St Jude's prosthesis. Two years after operation the child is fit and active. There have been no difficulties with anticoagulant treatment.
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The Authors describe a case of a patient suffering from mitral prolapse whose echocardiogram shows in addition to typical findings of this syndrome an annual systolic anterior motion (SAM) of the anterior mitral leaflet, generally present in the idiopathic hypertrophic obstructive cardiomyopathy and more seldom in some others disease, however not present in this present. The Authors suggest that this finding is correlated to the mitral prolapse and express some hypothesis regarding this possibility.
To determine the mitral valve abnormalities associated with hemodynamically important mitral regurgitation (MR) among patients with mitral valve prolapse (MVP), computerized 2-dimensional echocardiographic measurements of mitral leaflet and anular dimensions and motion in 26 patients with MVP and MR were compared to those in 48 subjects with uncomplicated MVP, 16 patients with MR due to etiologies other than MVP (rheumatic in 8) and 35 normal adults. Compared to both uncomplicated MVP and normal subjects, patients with MVP plus MR were older (p less than 0.05), had strikingly large mitral leaflets and anulus (p less than 0.0005) and were more likely to have systolic billowing of mitral leaflets in the parasternal long-axis view (24 of 26 [92%] vs 24 of 48 subjects with uncomplicated MVP [50%], p less than 0.001). Overlap in anular and posterior leaflet dimensions in normal and uncomplicated MVP subjects occurred in the 20 MVP plus MR patients who continue to be followed medically but not in the 6 MVP plus MR patients who underwent mitral valve surgery during 22 +/- 14 months follow-up. Patients with MR due to rheumatic or other non-MVP etiologies had enlargement of mitral leaflets and anulus virtually identical to that in MVP plus MR patients. In conclusion, patients with severe MR due to MVP are older, have striking mitral valve enlargement and more frequently exhibit leaflet billowing compared with subjects with uncomplicated MVP. Similar mitral leaflet enlargement was found in patients with non-MVP etiologies of MR, suggesting that mitral anular and leaflet enlargement may play a more general role in the pathogenesis of MR than is currently appreciated.
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BACKGROUND: Mitral valve repair for mitral valve regurgitation has many advantages over mitral valve replacement. However, durability and reoperation after mitral valve repair still remain major problems. We examined the outcome of mitral valve repair for mitral valve regurgitation and analyzed several pre- and intraoperative potential risk factors to determine the significant risk factors of reoperation. METHODS: From February 1981 to November 1996, 86 patients underwent mitral valve repair for mitral regurgitation or combined mitral regurgitation and stenosis. The mean age was 53 years, and 88.4% were New York Heart Association class III or IV. The causes of mitral valve disease were degenerative disease in 53 patients, rheumatic disease in 15, infective endocarditis in 11, and ischemic disease in 7. There were 2 early and 8 late deaths. RESULTS: Actuarial overall survival including early death at 10 years was 83.2+/-6.1%, freedom from reoperation was 86.8+/-5.3%, freedom from thromboembolism was 90.9+/-6.2%, and freedom from infective endocarditis was 98.5+/-1.5%. There was no bleeding event. At the last follow-up, most patients were in New York Heart Association class I or II. Prolapse of anterior leaflet and rheumatic mitral regurgitation were identified as independent predictors for reoperation. CONCLUSIONS: The repair techniques for anterior leaflet prolapse and patient selection in rheumatic mitral disease are important for improving long-term results of mitral valve repair for mitral regurgitation.
Primary mitral valve tumors are rare. We describe the transesophageal appearances of a papillary fibroelastoma (Lambl's giant excrescence) of the anterior mitral valve leaflet causing partial mitral valve obstruction. Transesophageal echocardiography proved particularly useful in identifying the limited attachment of the tumor to the anterior mitral valve leaflet and excluding its attachment to the interatrial septum. These features helped to exclude the possibility of the tumor being a left atrial myxoma, the primary differential diagnosis of the lesion. Transesophageal echocardiography enabled the planned surgical option to be mitral valve repair and also allowed intraoperative monitoring to assess the results of the surgical repair.
Over the past 40 years mitral valve surgery has changed dramatically. After initial enthusiasm with the introduction of valve prostheses in the 1960s, a renewed interest in repair techniques began in the 1970s with the introduction of annuloplasty rings. These repair techniques revealed that the integrity of the subvalvular apparatus plays an important role in left ventricular function. When considering the major series comparing early and late results of mitral valve repair versus prosthetic mitral valve replacement, operative mortality rate is lower for patients with mitral valve repair. Long-term results also show a superior survival rate after mitral valve reconstruction. In addition, several problems can occur with the prosthetic valve, such as thromboembolism and endocarditis. All of these factors favor valve repair over replacement. The success of mitral valve repair depends on many factors: etiology of the mitral valve disease and the resultant pathomorphology of the valve, patient's circumstances such as age or contraindication for anticoagulation, and the experience of the surgeon. The decision whether to repair or replace the mitral valve depends on these factors. Data in the literature and in large collective databases reflect the advantages of mitral valve repair, with over 75% of current mitral valve surgeries being repairs. In the past 5 years the exposure of the mitral valve through a right lateral minithoracotomy using video assistance has developed into a widespread technique. This approach allows complex mitral valve repair as well as mitral valve replacement even with biological stentless prostheses, with decreased morbidity. The addition of radiofrequency ablation for restoration of sinus rhythm enhances the outcome after mitral valve surgery, and can also be easily performed through a minithoracotomy technique.
A decrease in severity of rheumatic fever, in the number of recurrences of the disease, a relative decrease in prevalence of rheumatic heart disease compared to other forms of heart disease are well documented or suggested by the data collected in the last decades. The reasons of the decline are uncertain. Prevalence surveys in more recent years indicate that, while at one time almost all valvular heart disease was considered to be rheumatic in origin, current data suggest that a significant proportion of damaged valves may be attributed to congenital defects or to acquired disease of other etiologies. Bicuspid aortic valve and mitral valve prolapse deserve special mention. The main clinical and echocardiographic features of bicuspid aortic valve and mitral valve prolapse are discussed.
Mitral valve regurgitation frequently accompanies aortic valve stenosis. It has been suggested that mitral regurgitation improves after aortic valve replacement alone and that the mitral valve need not be replaced simultaneously Furthermore, mitral regurgitation associated with coronary artery disease, particularly in patients with poor left ventricular function, shows immediate improvement after coronary artery bypass grafting. We studied 60 consecutive patients with aortic stenosis and mitral regurgitation to determine the degree of improvement in mitral regurgitation after aortic valve replacement alone versus aortic valve replacement combined with coronary artery bypass grafting. Thirty-six of the patients had normal coronary arteries (Group 1); the other 24 had symptomatic coronary artery disease requiring bypass surgery (Group 2). Echocardiography was performed preoperatively, 1 week postoperatively, and at follow-up. In Group 1, left ventricular ejection fraction did not improve early or at 2.5 months postoperatively, but mitral regurgitation improved gradually during follow-up. In Group 2, mitral regurgitation showed improvement 1 week postoperatively (p < 0.001), and left ventricular ejection fraction was improved at 2.5 months. We conclude that patients with aortic valve stenosis and mild-to-severe mitral regurgitation, without echocardiographic signs of chordal or papillary muscle rupture and without coronary artery disease, should undergo aortic valve replacement alone. The mitral regurgitation will remain the same or improve. For patients with coexisting coronary artery disease, simultaneous aortic valve replacement and coronary artery bypass grafting are imperative; however, the mitral valve again requires no intervention, since mitral regurgitation improves significantly after the other 2 procedures.
To explore reasons for a high accumulation of Ca and P occurring in the coronary artery of Thai with aging, the authors investigated age-related changes of elements in the coronary artery, ascending aorta near the heart, and cardiac valves in single individuals, and the relationships in the elements between the coronary artery and either the ascending aorta or cardiac valves. After an ordinary dissection by medical students at Chiang Mai University was finished, the anterior descending arteries of the left coronary artery, ascending aortas, mitral valves, and aortic valves were resected from the subjects. The subjects consisted of 17 men and 9 women, ranging in age from 46 to 76 yr. The element content was analyzed by inductively coupled plasma-atomic emission spectrometry. The average content of Ca and P was the highest in the coronary artery and decreased in the order aortic valve, ascending aorta, and mitral valve. The Ca, P, and Mg content increased in the coronary artery in the fifties and in the ascending aorta, aortic valve, and mitral valve in the sixties. It should be noted that the accumulation of Ca, P, and Mg occurred earlier in the coronary artery than in the ascending aorta, aortic valve, and mitral valve. It was found that with respect to the Ca, P, Mg, and Na contents, the coronary artery correlated well with both the aortic valve and ascending aorta, especially with the aortic valve, but it did not correlate with the mitral valves. This finding suggests that the accumulation of Ca, P, Mg, and Na occurs in the coronary artery together with the aortic valve and ascending aorta, but not together with the mitral valve. Because regarding the accumulation of Ca, P, and Mg, the ascending aorta and aortic valve are preceded by the coronary artery, it is unlikely that the accumulation of Ca, P, and Mg spreads from the ascending aorta or aortic valve to the coronary artery.
To evaluate the role of the extent of calcific deposits on the anterior mitral leaflet in predicting the severity of mitral valve stenosis, two-dimensional echocardiography (2D Echo) and heart catheterization data were analysed in 62 patients with mitral valve stenosis, pure or associated with trivial valve regurgitation. 50 patients had technically adequate 2D Echo. Of these, 28 had pure mitral valve stenosis. The mitral valve area was estimated from the parasternal short-axis 2D Echo projection. Using the parasternal long-axis projection, calcium deposits location and extension on the anterior mitral leaflet was examined. Patients were subdivided into the following groups: Group 0 (absence of calcium deposits = 19 patients), Group 1 (calcium on distal third of the leaflet = 19 patients), Group 2 (calcium on mid and distal segments = 11 patients), Group 3 (calcium on the entire leaflet = one patient). The extension of calcium deposits in long-axis projection was contrasted with 2D Echo mitral valve area in the 50 mitral valve patients. 2D Echo and heart catheterization derived mitral valve area were compared to each other in the 28 patients with pure mitral valve stenosis. 2D Echo mitral valve area was greater in Group 0 patients (1.8 +/- 0.4 cm2) than in Group 1 (1.4 +/- 0.4 cm2) and in Group 2 (1.1 +/- 0.3 cm2) (p less than 0.001 between the three groups). Calcific deposits were present on the anterior mitral leaflet in 30/31 patients with 2D Echo mitral valve area less than or equal to 2 cm2. However, of the 19 patients of Group 0, 13 had moderate and one severe mitral valve stenosis. In the 28 patients with pure mitral valve stenosis, 2D Echo mitral valve area was excellently correlated with Gorlin's derived mitral valve area (r = 0.90). However, in patients with extensive calcification of the anterior mitral valve leaflet (Group 2), 2D Echo mitral valve area was significantly greater than the Gorlin's derived area (1.08 +/- 0.20 cm2 versus 0.68 +/- 0.17 cm2; p less than 0.001). In four patients of Group 2, the mitral valve stenosis was moderate by 2D Echo grading and severe by heart catheterization data. Our data suggest that the study of extension of calcific deposits on the anterior mitral valve leaflet may be a complementary aid in quantifying mitral valve stenosis to the 2D Echo mitral valve area estimate, especially when the valve is severely calcified.
Patients with mitral valve disease undergoing surgery are at an increased risk of thromboembolism. We hypothesized that this may be due in part to abnormalities in platelet activation, endothelial damage or dysfunction, and plasma fibrinogen in such patients. To test this hypothesis, we measured indexes of platelet activation (soluble P-selectin), endothelial damage or dysfunction (von Willebrand factor [vWf], enzyme-linked immunosorbent assay) and fibrinogen (modified Clauss) in 56 consecutive patients (35 women, mean age 65 years) admitted for isolated mitral valve repair (n = 39) or replacement (using mechanical implants, n = 17). Samples were taken from a peripheral vein before and at 3 months after valve surgery. Baseline results were compared with 56 healthy age- and sex-matched controls. Compared with controls, patients with mitral valve disease had higher levels of vWf (mean +/- SD 132 +/- 28 vs 101 +/- 35 IU/dl; p <0.001), but there were no significant differences in mean fibrinogen (p = 0.418) or soluble P-selectin (p = 0.855) levels between cases and controls. There was a significant increase in plasma vWf after mitral valve replacement: 142 +/- 25 IU/dl preoperatively, increasing to 161 +/- 33 IU/dl at 3 months after surgery (p = 0.0261). However, there were no significant changes in plasma fibrinogen (p = 0.306) or soluble P-selectin levels (p = 0.191). Patients undergoing mitral valve repair did not have any significant changes in mean vWf (p = 0.25), soluble P-selectin (p = 0.77), or fibrinogen (p = 0.22). There was a significant negative correlation (Spearman, r = -0.4, p = 0.003) in postoperative plasma vWf levels and the size of valve prosthesis used. Thus, patients with mitral valve disease have increased plasma vWf levels when compared with healthy controls, suggesting endothelial damage or dysfunction, with a further increase in levels after mitral valve replacement. Conversely, patients undergoing mitral valve repair do not demonstrate any significant changes in fibrinogen, or indexes of endothelial dysfunction or platelet activation.
BACKGROUND: Patients with ischemic mitral incompetence have a high operative risk whether the valve is repaired or replaced. The advantage of repair over replacement is unclear in this group of patients. METHODS: Between April 1986 and December 1994, 232 patients underwent surgery for ischemic mitral valve insufficiency; mitral valve replacement was performed in 98 of them. Operative mortality was 13.3%. The actuarial survival rate after 5 years was 73.3%. The surgical risk in patients whose left ventricular ejection fraction (LVEF) was 10%-30% (operative mortality 50.0%) was higher than in those whose LVEF was greater than 30%. Valve reconstruction was performed in 102 patients. Operative mortality in this patient group was 14.7%. The surgical risk in patients whose LVEF was < or = 30% was higher (operative mortality 42.9%). RESULTS: The total actuarial survival rate of all patients was 64.4% after 5 years. Mortality during follow-up was higher in patients with residual mitral valve insufficiency greater than grade I after mitral valve reconstruction. Twenty-four patients with severely impaired left ventricular function underwent heart transplantation. Operative mortality in this group was 12.5%. Eight patients received left ventricular aneurysmectomy in addition to valve surgery, three of them died early. CONCLUSIONS: We conclude that patients with highly impaired left ventricular function and ischemic mitral insufficiency are at too great a risk for either valve reconstruction or replacement. Cardiac transplantation should be considered for this patient group. However, patients with ischemic mitral insufficiency and moderately impaired left ventricular function can undergo valve reconstruction or replacement with an acceptable prognosis. The goal of mitral valve reconstruction should be reducing mitral valve insufficiency to at least grade I. If this is not achieved, the prognosis after repair is worse than after valve replacement, therefore, the surgeon should replace the valve without delay.